Xu Fei, Wu Qiong, Yang Yishu, Zhang Ling, Yan Zhen, Li Huijun, Li Juan, An Zhen, Wu Hui, Song Jie, Wu Weidong
School of Public Health, Xinxiang Medical University, Xinxiang, China.
International School of Public Health and One Health, Hainan Medical University, Haikou, China.
Sci Total Environ. 2023 Dec 10;903:166795. doi: 10.1016/j.scitotenv.2023.166795. Epub 2023 Sep 4.
Short-term exposure to ozone (O) has been associated with airway inflammation. Given that high temperature (HT) accelerates O production, it is of significance to determine whether co-exposure to HT exacerbates O-induced airway inflammation. The aim of this study was to examine the possible promotive effect of HT on O-induced airway inflammation and underlying mechanisms. Forty-eight C57BL/6 N male mice were randomly divided into four groups: filtered air (control), O, HT, and HT + O (co-exposure) groups. Mice in control and O groups were exposed to filtered air or 1 ppm O at 24 °C, respectively, while mice in HT and co-exposure groups were exposed to filtered air or 1 ppm O at 36 °C, respectively. The exposure scenario for four groups was 4 h/d for 5 consecutive days. Bronchoalveolar lavage fluids (BALF) were collected 24 h after the last exposure and subjected to examinations of oxidative stress and inflammation biomarkers, 16S rRNA sequencing, and metabolic profiling. Lung tissues were processed for H&E histological staining. The results showed that O inhalation triggered oxidative stress and inflammation in the airways, which was worsen by co-exposure to HT. Further studies revealed that co-exposure to HT strengthened O-induced decline in Firmicutes and Allobaculum in airways. Moreover, co-exposure to HT promoted O-induced airway metabolic disorder. Spearman correlation analysis revealed correlations among microbiota dysbiosis, metabolic disorder, oxidative stress and inflammation induced by co-exposure to HT and O. Taken together, HT exposure aggravates O-induced airway oxidative stress and inflammation, possibly through modulation of microbiota and metabolism of the airways.
短期暴露于臭氧（O₃）已被证实与气道炎症有关。鉴于高温（HT）会加速O₃的产生，因此确定HT与O₃共同暴露是否会加剧O₃诱导的气道炎症具有重要意义。本研究的目的是探讨HT对O₃诱导的气道炎症的可能促进作用及其潜在机制。48只C57BL/6 N雄性小鼠被随机分为四组：过滤空气（对照组）、O₃组、HT组和HT + O₃（共同暴露）组。对照组和O₃组的小鼠分别在24℃下暴露于过滤空气或1 ppm O₃，而HT组和共同暴露组的小鼠分别在36℃下暴露于过滤空气或1 ppm O₃。四组的暴露方案均为连续5天，每天暴露4小时。在最后一次暴露后24小时收集支气管肺泡灌洗液（BALF），并对其进行氧化应激和炎症生物标志物检测、16S rRNA测序以及代谢谱分析。对肺组织进行苏木精-伊红（H&E）组织学染色。结果表明，吸入O₃会引发气道中的氧化应激和炎症，而HT与O₃共同暴露会使其恶化。进一步研究表明，HT与O₃共同暴露会加剧O₃诱导的气道中厚壁菌门和Allobaculum菌属的减少。此外，HT与O₃共同暴露会促进O₃诱导的气道代谢紊乱。Spearman相关性分析揭示了HT与O₃共同暴露所诱导的微生物群失调、代谢紊乱、氧化应激和炎症之间的相关性。综上所述，HT暴露可能通过调节气道微生物群和代谢来加剧O₃诱导的气道氧化应激和炎症。
